This study proposes to show that a loss in lung elastic recoil has two mechanisms; 1) an increase in resting tissue length (Lo) and 2) a loss in number and volume density of elastic elements (emphysema). Furthermore, it will show that emphysema is not a single entity. The pressure-volume (P-V) characteristics accompanying a localized loss in tissue (centrilobular (CLE) being different in shape and sensitivity from that seen in lungs with a diffuse tissue loss (panlobular (PLE). Since these mechanisms may act singly or in concert, failure to recognize a change in Lo or the difference between types of emphysema may leave the loss in recoil unexplained. Structural criterion for the recognition of the Lo change are to be developed. The mechanisms are to be studied in aging human lungs and those with increasing degrees of emphysema. The length-tension (L-T) properties of parenchyma and the P-V characteristics of each lung in air and saline will be measured directly and compared with the morphologic and morphometric measures in the same lung. From the L-T and structural data we can calculate the deflation P-V characteristics. The calculated deflation curves can be compared with the measured P-V curves to assess the contribution of the tissue property change in the presence of CLE or PLE. Structural criterion for recognizing the change in Lo will be introduced into these calculations for comparison.